Burchfield D M, Rall J A, Rahwan R G
Am J Physiol. 1982 May;242(5):C347-52. doi: 10.1152/ajpcell.1982.242.5.C347.
Mechanical and energetic effects of 2-n-butyl-3-dimethylamino-5,6-methylenedioxyindene (2-butyl-MDI) were investigated in isolated frog semitendinosus muscles at 0 degrees C. Previous research on various tissues suggested that this compound functions as an intracellular Ca2+ antagonist. The effects of 2-butyl-MDI (2 X 10(-4) M) with respect to time were progressive and reversible with exposures of 30 min or less. A 30-min exposure to the agent significantly decreased twitch and tetanus force and energy liberation, increased the twitch-to-tetanus ratio, prolonged kinetics of force development, induced a stimulus frequency-dependent tetanic fatigue, and decreased contractile economy (measured as force per unit energy liberation). Energy associated with Ca2+ cycling, activation heat, was depressed by 31 +/- 4%. The significant reduction of activation heat production by 2-butyl-MDI suggests that the quantity of Ca2+ released by the sarcoplasmic reticulum upon stimulation is reduced. However, the complexity of the results summarized above suggests multiple sites and/or modes of action for the agent.
在0摄氏度下，对离体青蛙半腱肌研究了2-正丁基-3-二甲氨基-5,6-亚甲基二氧茚（2-丁基-MDI）的机械和能量效应。先前对各种组织的研究表明，该化合物作为细胞内Ca2+拮抗剂发挥作用。2-丁基-MDI（2×10^(-4) M）的效应随时间逐渐显现且可逆，暴露时间在30分钟或更短。暴露于该药剂30分钟显著降低了单收缩和强直收缩力以及能量释放，增加了单收缩与强直收缩的比率，延长了力发展的动力学过程，诱发了刺激频率依赖性的强直疲劳，并降低了收缩效率（以单位能量释放产生的力来衡量）。与Ca2+循环相关的能量，即激活热，降低了31±4%。2-丁基-MDI使激活热产生显著降低，这表明刺激时肌浆网释放的Ca2+量减少。然而，上述结果的复杂性表明该药剂存在多个作用位点和/或作用模式。
